Assessment of ischemia and reperfusion injury

Direct videomicroscopy of the rat cremaster muscle microcirculation supplemented by animal models of replantation, vascular crushing, and muscle function after injury and recovery were used to investigate the occurrence of reperfusion failure. It is evident that failure of blood reflow may be induced by multiple factors that can be grouped into categories of ischemia, intimal damage, and systemic or local responses, which are referred to as the no reflow triad. The components comprising the 3 sides of the no reflow triad can interact with one another in an intricate manner, and any single factor or combination of factors is capable of triggering the events leading to reperfusion failure. The pronounced regional nature of reperfusion injury and the direct relationship between the severity of the observed vascular alterations and increasing duration of ischemia have been documented. The dynamic changes and histopathology of the microcirculation included constriction of the arteries, swelling of endothelial and leukocytes, and erythrocyte rouleaux formation during ischemia. As ischemia duration was lengthened, the degree of these changes increased correspondingly. The changes on reperfusion were disruption of blood flow patterns, vortex formation, regional stasis, adhesion and migration of leukocytes, focal hemorrhage, edema, vasospasm, and platelet aggregation. The deleterious effects of systemic acidosis, interstitial hemorrhage, denervation, and prolonged venous occlusion were subsequently documented. The application of information gained from this series of laboratory experiments has resulted in continued improvement in the success rate in clinical microvascular surgery.